Block 9 Week 5

Krishnan Pathophysiology of Cardiac Arrhythmias Lecture Notes

Three Major Mechanisms of Cardiac Arrhythmias
1. Enhanced Automaticity
Increased rate of firing of cardiac pacemaker cells (by increasing the slope of phase 4 depolarization)
The slope is increased by sympathetic stimulation or beta-stimulation
Best example is sinus tachycardia
Abnormal automaticity can occur in cells that normally lack spontaneous depolarization and can cause
premature atrial contractions (PACs) as well as premature ventricular contractions (PVCs)
2. Triggered activity and afterdepolarizations
When an abnormal afterdepolarization is large enough to reach threshold potential, it will trigger a new
action potential
Afterdepolarizations occur when there is an increase in Ca2+ concentrations (as seen with excess
catecholamines, increased cAMP, or myocardial ischemia)
When one triggered AP occurs, it is frequently followed by a long run of triggered Aps, each arising from
new afterdepolarizations
o Digitalis toxicity can induce these arrhythmias
o Anti-arrhythmic drugs that prolong the duration of APs in Purkinje fibers can induced early
afterdepolarizations; prolonged QT intervals can also induce early afterdepolarizations
o Anti-arrhythmic drugs that shorten the duration of the AP should help prevent triggered activity
due to afterdepolarizations
3. Re-entry (circus movement)
Most common mechanism underlying clinical tachyarrhythmias
Situation where an impulse can re-enter and depolarize a region of myocardium a second time without
another impulse from the pacemaker
Requires three things
o A unidirectional block of an electrical impulse
o Slow conduction of the AP impulse in one part of the circuit
o Refractoriness among regions of the circuit
Macro-entry arrhythmias tend to be more organized and anatomical and the pathways are fixed
o AV nodal re-entry
o Atrioventricular re-entry using the bundle of Kent causing a slurred QRS upstroke known as a
delta wave (WPW syndrome)
o Right atrial re-entry in atrial flutter
o Ventricular tachycardia following MI-induced scarring
o Bundle branch re-entry
Micro-entry arrhythmias tend to be more dynamic and variable and are often caused by ischemia
o Atrial fibrillation
o Ventricular fibrillation
o Polymorphic ventricular tachycardia (Torsades de pointe)
Treatment
o Drugs that slow the impulse conduction through slowed conduction pathways so much that the
propagation just dies out (Ca2+-channel blockers and adenosine)

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